Links for Keyword: Parkinsons

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ST. PAUL, MN -- Women who consume little or no caffeine, but who take hormone replacement therapy, may reduce their risk of developing Parkinson’s disease, according to a study published in the March 11 issue of Neurology, the scientific journal of the American Academy of Neurology. However, HRT may increase disease risk in women who drink the equivalent of more than five cups of coffee per day. Two large studies have previously shown that increased caffeine intake is associated with a lower risk of Parkinson’s disease in men. Studies in women, which to date have not factored in use of hormone replacement therapy, have been contradictory and inconclusive. Parkinson’s disease is less common in women, and some evidence suggests that estrogen may help protect the neurons that degenerate in this disease. Estrogen is the principal hormone in HRT, a common therapy in post-menopausal women.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 8: Hormones and Sex
Link ID: 3587 - Posted: 06.24.2010

ST. PAUL, MN – Previous research has implicated oxidative damage (cell degradation) in the development of Parkinson’s disease. Because vitamins E, C and carotenoids are antioxidants, researchers recently studied the associations between their intake and risk of Parkinson’s disease. Their conclusions point not to supplements, but to dietary intake of vitamin E (from the foods we eat) as having a protective factor in the risk of developing Parkinson’s disease. The study is reported in the October 22 issue of Neurology, the scientific journal of the American Academy of Neurology. Using repeated and validated dietary assessments of two large study cohorts, researchers from Harvard School of Public Health, Brigham and Women’s Hospital, and Harvard Medical School examined the associations between dietary intakes of vitamin E, C, and carotenoids, vitamin supplements, and risk of Parkinson’s disease. After exclusions, 76,890 women from the Nurses’ Health Study (NHS) and 47,331 men from the Health Professionals Follow-Up Study (HPFS) were included in the study analyses.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 2906 - Posted: 06.24.2010

In the first study of its type, researchers at Emory University and nine other centers nationwide have determined that a naturally occurring compound called coenzyme Q10 can slow progressive deterioration associated with the early stages of Parkinson's disease up to 44 percent. This is the first time a study has shown that any nutrient or vitamin might play a role in slowing the progression of PD. The greatest benefits were seen in motor skills and activities of daily living, such as walking, dressing, feeding and bathing. The results of this study will be published in the Oct. 15 issue of the American Medical Association's Archives of Neurology and will be discussed at the annual meeting of the American Neurological Association in New York City, also on Oct. 15. "The study was designed to test the hypothesis that high doses of coenzyme Q10 would slow the progression of Parkinson's, as measured by movement difficulty or disability," says Ray Watts, M.D., professor of neurology, Emory University School of Medicine, and lead investigator of the Emory study. "We are very encouraged with the results of this small trial, which consisted of 80 Parkinson's patients nationwide. However, a larger, multi-centered, controlled trial is still needed before this treatment can be recommended to patients with a high degree of certainty."

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 2801 - Posted: 06.24.2010

UCLA scientists have developed a fast new way to image how thousands of genes misfire proteins in a mouse model of Parkinson’s disease. The approach may provide a research blueprint for pinpointing the abnormal brain regions linked to autism and schizophrenia. The new findings are reported in the June edition of Genome Research. Last year, UCLA pharmacologist Desmond Smith developed a new method to rapidly track how genes express proteins in the human brain. Called “voxelation,” the approach involves cutting the brain into cubes, then using DNA chip technology and math to reconstruct gene expression patterns in three-dimensional images. This time, Smith used voxelation to compare gene expression in the brains of mice. Half of the mice received drugs to induce Parkinson’s disease. The UCLA team analyzed the brain cubes with DNA chips to track the expression of 9,000 genes simultaneously. They then combined the 9,000 resulting images to visualize how the genes construct the brain.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 2165 - Posted: 06.24.2010

Researchers at Emory University and a group of international collaborators, using positron emission tomography (PET) brain imaging, have determined that a relatively new drug slows the loss of dopamine function in early stages of Parkinson’s disease (PD) compared with an older, more commonly used drug. Investigators say the drug ropinirole (brand name ReQuip ) slows the loss of dopamine, a neurotransmitter produced by neurons in the brain that is found in steadily decreasing amounts as the disease progresses, in a more effective manner than levodopa (brand name Sinemet ). In this trial, the progression of the loss of dopamine function was slowed by over 30 percent in participants taking ropinirole as compared with participants in a comparable stage of the disease taking levodopa.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 1893 - Posted: 06.24.2010

By Julia Sommerfeld MSNBC DENVER, — Experimental transplants of cells from aborted fetuses and donated eyes are showing promise for the treatment of Parkinson’s disease, according to two studies out Wednesday. Both types of cells were shown to survive in patients’ brains and improve some of the hallmark symptoms of the dreaded disease. PARKINSON’S, which affects an estimated 1 million people in the United States, is caused when the brain cells that produce a chemical known as dopamine die off. Colorado researchers reported follow-up results on a controversial experiment in which holes were drilled in the skull and dopamine cells from aborted fetuses were implanted in the brains of advanced Parkinson’s patients. Other doctors described the initial results of transplants of dopamine cells from the retinas of donated eyes. Both findings were presented at the annual meeting of the American Academy of Neurology in Denver. “It takes the loss of 80 percent to 90 percent of dopamine-producing neurons to lead to the symptoms of Parkinson’s disease,” said Dr. Robin Brey, a professor of medicine, division of neurology at University of Texas Health Sciences Center, San Antonio. “So you need fairly small amount of dopamine-producing neurons to remain normal. That tells us that even if a small number of transplanted cells were to take and produce dopamine, that could do a lot. So this is very promising.” MSNBC Terms, Conditions and Privacy © 2002

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory, Learning, and Development
Link ID: 1902 - Posted: 06.24.2010

By Stacey Singer Health Writer It would cost $100,000 for the operation that could stop her mother’s tremors. No one in the family had that kind of money, and there was no health insurance. Grace Donofrio knew all this as she scanned the Internet, reading about the latest surgical treatment for tremors caused by Parkinson’s disease. It was early in 2001, and Donofrio, full of hope, called a family meeting. She told her brother and sister that no matter what it cost, no matter what they had to sell or borrow, they must find a way to give their mother the operation. Somberly, they all agreed. In her healthy days, Neponezia Simoes crafted beautiful dresses, an elegant confection of organdy and flowers for Donofrio’s wedding, a variation of Chanel or St. Lauren for a regular customer. Copyright © 2001, South Florida Sun-Sentinel

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 1217 - Posted: 06.24.2010

By Ingrid Wickelgren If your hands and arms quiver when you write and do other tasks, you may have a common neurological condition called essential tremor (ET). As many as 7 percent of adults older than 65 suffer from ET, which may also affect the head and voice. In severe cases, it can be disabling. The cause of such shaking has long been mysterious. But researchers are beginning to uncover a biological explanation for the problem: they have found a gene that may contribute to its development as well as a pathological signature of the disorder in the brain. Researchers knew that genetic factors underlie ET, as half or more of the cases run in families. But no one until now had succeeded in nabbing any of the responsible genes. To find such a gene, scientists at deCODE genetics in Iceland compared DNA blueprints from hundreds of tremor patients and thousands of unafflicted residents. In each person’s DNA, researchers looked at 305,624 single-nucleotide polymorphisms (SNPs), sites where the identity of the chemical unit (the pair of molecules that makes up each building block of a strand of DNA) commonly varies among people. Out of that analysis emerged one SNP that consistently differed between the patients and the others. The same chemical unit also turned out to be tied to ET in populations of patients whom the researchers recruited from Germany, Austria and the U.S. The newly fingered SNP lies in a gene for a protein called LINGO1 that is present only in the brain and spinal cord—a distribution consistent with a role in neurological disorders, says neurologist Dietrich Haubenberger of the Medical University of Vienna in Austria, one of the study’s authors. The protein, which straddles the cell membrane, is thought to govern interactions among cells and to thereby influence neuronal integrity as well as function. LINGO1 also has been implicated in multiple sclerosis and Parkinson’s disease, but its precise role in these disorders and in ET is unclear. © 1996-2009 Scientific American Inc.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 13149 - Posted: 06.24.2010

By DARCY HELLER STERNBERG I can spot Marty in a crowd a block away. He tilts left into the wind, as if he were shouldering the full blast of Hurricane Katrina, his arm gesticulating awkwardly. Once a well-dressed woman asked if I had seen “that man — I think he’s drunk.” I assured her the man was my husband. “He has Parkinson’s,” I told her. We get that a lot — snickers, whispers. Looks that wound. “When people stare,” Marty tells me, “I get nervous and shake that much more.” There are no rules of etiquette for dealing with a person who has a neurological disorder. Some people do stare; others recoil. Fortunately, though, many are genuine and forthcoming in their help. And that is as true here in New York City, supposedly the capital of heartless impatience, as it is anywhere in the country. Marty has to take a combination of seven drugs eight times a day. He bought an expensive pillbox specifically made for Parkinson’s patients; an alarm goes off when it’s time to take a pill. One problem: the container is so difficult to open that when he finally succeeds, the pill is likely to go flying across the room or, worse, into the street. Even when he’s able to grasp the pill and take it, it may not last as long as he would like. “After a few years of taking medication, people with Parkinson’s may begin to experience ‘wearing off’ spells,” Dr. Lawrence I. Golbe, a neurologist at Robert Wood Johnson University Hospital in New Brunswick, N.J., recently wrote in the Parkinson’s Disease Foundation newsletter, adding that for some patients the drugs may be effective for only three hours. Copyright 2009 The New York Times Company

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 12749 - Posted: 06.24.2010

by Jessica Hamzelou Boosting brain waves can make people move in slow motion. This finding is one of the first to show that brain waves directly influence behaviour, and it could lead to new treatments for Parkinson's disease and other disorders that affect movement. Peter Brown and his colleagues at University College London generated a small electrical current in the brains of 14 healthy volunteers using scalp electrodes. The current increased the activity of normal beta waves – a kind of brain wave that is usually active during sustained muscle activities, such as holding a book. Beta activity usually drops before people begin a movement. The participants then carried out a simple task: they moved a spot on a computer screen as quickly as possible using a joystick. When beta wave activity increased, their fastest times slowed by 10 per cent. "This is the first time that beta wave activity has been shown to slow movement," Brown says. Other studies have found that people with Parkinson's disease have greater beta activity. Brown's research suggests this could be linked to the slowing of movement seen in those with the disease. Electrical stimulation deep in the brain is used to treat people with Parkinson's, although how it works is a subject of debate. © Copyright Reed Business Information Ltd

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 10: Biological Rhythms and Sleep
Link ID: 13321 - Posted: 06.24.2010

Peter Aldhous Therapeutic cloning works – in mice, at least. An international team has restored mice with a condition similar to Parkinson's disease back to health, using neurons grown in the lab that were made from their own cloned skin cells. This is the first time that a disease has been successfully treated using cloned cells that had been derived from the recipient animals. "It is the proof of concept," says Lorenz Studer of the Sloan-Kettering Institute in New York, US, who led the research. But he warns that is too early to say whether the technique can be developed into a practical therapy for human patients. Studer's team first gave mice a drug to kill neurons that make the neurotransmitter dopamine. This caused movement problems similar to those seen in people with Parkinson's disease. Then the researchers took biopsies from the tails of these mice and shipped them to Teruhiko Wakayama, a specialist in cloning at the RIKEN Center for Developmental Biology in Kobe, Japan. Wakayama's team transferred the nuclei from skin cells taken from these biopsies into mouse eggs stripped of their chromosomes, to create embryos. The Japanese researchers extracted embryonic stem (ES) cells from these cloned embryos, creating a total 187 ES cell lines from 24 mice. © Copyright Reed Business Information Ltd

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 11459 - Posted: 06.24.2010

Human trials of isradipine (or DynaCirc) – which is prescribed for hypertension and stroke – are now planned. Over time, Parkinson's patients lose a set of brain cells that produce the crucial signalling chemical dopamine – and these cells do not regenerate. Without enough dopamine, people cannot control their body movements and ultimately develop severe neurological problems, including dementia. Scientists have struggled to understand why the dopamine-producing brain cells start dying, but ageing plays a strong role. James Surmeier at Northwestern University in Illinois, US, and colleagues found that in young mice these cells use sodium channels to send signals, but in older mice they rely more on a certain kind of calcium channel. This can prove deadly for a neuron because calcium accumulates inside the cell, eventually triggering a complete breakdown. Surmeier wondered whether he could reverse the switch to calcium channels: "The cells had put their old childhood tools in the closet. The question was, if we stopped them from behaving like adults, would they go into the closet and get them out again?" © Copyright Reed Business Information Ltd

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 10395 - Posted: 06.24.2010

By Michael Day People with Parkinson's disease are three times more likely than non-sufferers to have been troubled by allergic rhinitis – an inflammatory nasal response to pollen or other airborne particles – a new study finds. The results suggest that allergic diseases, such as hay fever, may be linked to brain inflammation that hastens the onset of the neuro-degenerative disorder, say researchers at the Mayo Clinic in Rochester, Minnesota, US. Previous studies have shown that non-steroidal anti-inflammatory drugs, such as ibuprofen, offered some protection against Parkinson's disease. These results prompted clinical neurologist James Bower and colleagues to investigate the links between inflammatory conditions and Parkinson’s disease. They studied 196 people with Parkinson’s disease and 196 others matched for age and gender. A comparison of the two groups revealed that those with Parkinson’s were 2.9 times more likely to have suffered rhinitis earlier in their lives. "People with allergic rhinitis mount an immune response with their allergies, so they may be more likely to mount an immune response in the brain as well, which would produce inflammation," Bower says. © Copyright Reed Business Information Ltd

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 11: Emotions, Aggression, and Stress
Link ID: 9223 - Posted: 06.24.2010

ST. PAUL, Minn. – People with Parkinson disease can be apathetic without being depressed, and apathy may be a core feature of the disease, according to a study published in the July 11, 2006, issue of Neurology, the scientific journal of the American Academy of Neurology. Apathy is a mental state characterized by a loss of motivation, loss of interest, and loss of effortful behavior. In apathy, the mood is neutral and there is a sense of indifference. In depression, the mood is negative and there is emotional suffering. Because apathy and depression share some of the same symptoms, the disorders can be misdiagnosed. “This study shows that it’s important to screen for both apathy and depression so patients can be treated appropriately,” said study author Lindsey Kirsch-Darrow, MS, of the University of Florida in Gainesville. “It will also be important to educate family members and caregivers about apathy to help them understand that it is a characteristic of Parkinson disease. Apathetic behavior is not something the patient can voluntarily control, and it is not laziness or the patient trying to be difficult – it is a symptom of Parkinson disease.” The study compared 80 people with Parkinson disease to 20 people with dystonia, another movement disorder. The researchers hypothesized that apathy would occur more often in people with Parkinson disease, because the disease affects areas of the brain in the frontal cortex that are involved in non-motor activities, whereas dystonia affects areas mainly involved with movement.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 9162 - Posted: 06.24.2010

RICHLAND, Wash.--Parkinson's, Alzheimer's, Lou Gehrig's disease and other brain disorders are among a growing list of maladies attributed to oxidative stress, the cell damage caused during metabolism when the oxygen in the body assumes ever more chemically reactive forms. But the precise connection between oxidation and neurodegenerative diseases has eluded researchers. Now, a study by the Department of Energy's Pacific Northwest National Laboratory and UCLA's David Geffen School of Medicine reveals that damage is linked to a natural byproduct of oxidation called nitration. "We looked at a healthy brain and found nitration of proteins that are implicated in neurodegenerative disease," said Colette Sacksteder, PNNL scientist and lead author of the study, published in the July issue of the journal Biochemistry (online Wed., June 28). PNNL scientist Wei-Jun Qian was co-lead author. The results are from the most detailed proteomic analysis of a mammalian brain to date – that is, a survey of nearly 8,000 different, detectable proteins in the mouse brain. The research suggests that many neurodegenerative diseases leave a biochemical calling card, or biomarker, that could be used to predict the earliest stages of brain impairment. Many biomedical researchers believe that detecting disease states before symptoms occur is the key to reversing many as-yet-incurable diseases.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 9070 - Posted: 06.24.2010

CHICAGO – Eleven patients with Parkinson's disease (PD) developed pathological gambling behavior following dopamine agonist therapy, a drug therapy to control movement problems caused by Parkinson's disease, according to a study posted online today which will appear in the September print issue of Archives of Neurology, one of the JAMA/Archives journals. Parkinson's disease, a degenerative disorder marked by the death of the neurons of an area of the brain called the substantia nigra, is primarily treated by drugs that restore or improve brain chemical signaling system dependent on dopamine, according to background information in the article. Brain dopamine, a chemical that helps regulate movement, balance and walking, also plays a central role in the behavioral reward system, reinforcing a myriad of behaviors. It has been implicated in the reward of gambling behavior. M. Leann Dodd, M.D., of the Mayo Clinic, Rochester, Minn., and colleagues, present reports of eleven patients seen and evaluated between 2002 and 2004 in the Mayo movement disorders clinic with Parkinson's disease who had recently developed pathological gambling and review similar cases from the medical literature. Pathological gambling is defined as a failure to resist gambling impulses despite severe personal, family or vocational consequences

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 7628 - Posted: 06.24.2010

A drug that relieves the symptoms of Parkinson’s disease – but was controversially withdrawn over toxicity fears – has now been shown to stimulate growth of the nerve fibres damaged by the disease. When delivered directly to the brain, glial cell-line derived neurotrophic factor (GDNF) had been shown to stimulate regrowth of cells in animal models of Parkinson’s. But this is the first time regrowth has been seen in the human brain, says Steven Gill, a neurosurgeon at Frenchay Hospital, Bristol, UK. Gill was running a trial study where five patients with advanced Parkinson’s disease were fitted with a tiny catheter that delivered GDNF direct to the putamen, part of the basal ganglia in the centre of the brain. In the putamen of Parkinson’s patients the chemical messenger dopamine is lost. The symptoms of Parkinson’s - which include uncontrollable shaking and trembling - were reduced in all five patients. They showed dramatic improvements with respect to their motor skills, verbal memory, facial expressions and motivation. However, Amgen, the company that makes GDNF, withdrew the drug after fears over its toxicity and a second trial of 34 patients was halted. That was despite the fact that the toxicity trials involved testing far higher doses of GDNF on animal models, and that none of the human subjects had showed any ill-effects. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory, Learning, and Development
Link ID: 7585 - Posted: 06.24.2010

DALLAS – Researchers at UT Southwestern Medical Center have discovered a mechanism that causes a protein to clump together in brain cells of people with Parkinson's disease, pointing toward a possible treatment for the condition. The protein clumping is part of a "vicious cycle," the researchers said. As the proteins cluster, they inhibit an enzyme that normally breaks them down, leading to the formation of even more masses. "It's a disease involving accumulation of a protein in an aberrant form," said Dr. Philip Thomas, professor of physiology at UT Southwestern and senior author of the study. The research, available online, was published in the June 17 issue of The Journal of Biological Chemistry. The findings have parallels to other diseases in which protein clusters form in and around nerves, such as Huntington's and Alzheimer's disease. The culprit in Parkinson's is the protein alpha-synuclein, which normally appears in a long, folded form in cells. It's known to be linked to the disease because mutations in it cause rare, inherited cases of early-onset Parkinson's. Normally, if a cell becomes stressed, alpha-synuclein unfolds, and an enzyme degrades it completely into harmless bits to prevent the clumping. In Parkinson's patients, however, some of the degrading enzyme malfunctions and creates truncated fragments of alpha-synuclein rather than the harmless bits.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 7533 - Posted: 06.24.2010

CHICAGO – Deep brain stimulation of two different areas of the brain appears to improve problems with uncontrolled movements (dyskinesia) in patients with Parkinson disease (PD), according to an article in the April issue of Archives of Neurology, one of the JAMA/Archives journals. Deep brain stimulation with electrical impulses delivered to structures deep within the brain is being intensively investigated for the management of advanced Parkinson disease, according to background information in the article. Although a number of studies have shown that stimulation of two different areas of the brain, the globus pallidus interna (GPi) and the subthalmic nucleus (STN), can be achieved safely and effectively, STN has been thought to be the preferred target. At the same time, the authors note, there does seem to be some evidence that the STN is more vulnerable during surgery and that STN patients may have more postoperative problems. Valerie C. Anderson, Ph.D., of the Oregon Health and Science University, Portland, and colleagues compared 23 patients with Parkinson disease and problems with medication-induced uncontrolled movement who were randomly assigned to implantation of deep brain stimulators in either the GPi or the STN areas of the brain. Patients' Parkinson symptoms were evaluated with and without medication using a standard rating scale at three, six and 12 months after surgery.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 7172 - Posted: 06.24.2010

INDIANAPOLIS – A mutation in a recently discovered Parkinson's disease gene is believed to be the most common genetic cause of inherited forms of the disease, according to a Parkinson Study Group study appearing in The Lancet in January. Researchers say the mutation on the LRRK2 gene is responsible for 5 percent of inherited Parkinson's disease cases. Tatiana Foroud, Ph.D., associate professor of medical and molecular genetics at Indiana University School of Medicine and principal investigator on the multi-site study, said the discovery has a broad implication for genetic screening for the disease. "Our results suggest that the mutation we have studied is the most common cause of Parkinson's disease identified to date," said Dr. Foroud. "While a great deal of work remains to be done, it is clear that any future genetic testing for Parkinson's disease must include studies of the LRRK2 gene." The patients in the Indiana University study who had the mutation had longer disease duration but less severe symptoms when they were participating in the trial. That suggests that the mutation may be associated with slower disease progression, said Dr. Foroud.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 6710 - Posted: 06.24.2010